You need to get calories from somewhere, should it be from carbohydrate or fat?

Tuesday, October 13, 2009

More from Japan

I was googling for an idea of what the current value is for LDL in the general population of the USA at the moment, when I accidentally hit on this paper. It's from the Japan cohort of the infamous Seven Countries Study, focusing on the farming town of Tanushimaru. Apart from the data presented, which are fascinating, there are the data not presented, which say a great deal more. What is also fascinating is the fossilised mindset of the investigators, inheriting from Ancel Keys the ability to look at, and in this case publish, data which destroy the lipid hypothesis as proposed by Keys so many years ago, but ignore what they have found. Lets look at some results tables.

The pdf is copy protected so if you would like the actual data just download the pdf and have a look-see.

I'll start with line one of Table 1, energy intake. This has fallen significantly between 1958 and 1999. Over that period BMI has risen from (Table 3) 21.7 to 23.7. The paper talks about less manual labour etc, suggesting BMI is some simplistic marker of calories in vs calories out. Duh. OK, people on the 1999 diet are storing more energy than they can access, compared to the massive caloric intake in 1958, which was being accessed at a rate which maintained a lower BMI. This to me suggests that the population in 1999 has a higher average insulin level despite lower carbohydrate intake. Think metabolic syndrome, not calories in vs calories out.

You would expect people with lower carbohydrate intake to have lower insulin levels, but anyone who follows Stephan's blog or any of the Kitava posts here will realise that very high carbohydrate diets per se are not the problem. The problem is failure to maintain efficient glucose usage at physiological concentrations of insulin. Something happened between 1959 and 1999 to increase insulin levels despite lowered carbohydrate intake. This means insulin resistance.

So the next thought is; what question do the investigators not ask, or at least not tell us so, if they did?

Table 1 tells us that in 1958 the farmers were eating 2837kcal/d, 84% of which was carbohydrate, ie 2383kcal of carbs. Flicking to table 2 we can see they were eating 593g/d of rice, ie 2668kcal of rice!!!!!!!!!!!!!!!! OK, they were eating more rice calories than carbohydrate calories! The numbers don't quite balance but this is not banking (jk) we're talking here. Assessing dietary intakes and the associated calories is not hard science and these researchers are not exactly famous for precision. Essentially all of this caloric intake was starch. I don't see a lot of scope for fructose intake when you are eating more rice calories than carbohydrate calories!

The same numbers in 1999 were 1365kcal as carbs and only 1062kcal of rice. There is now a deficit of 300kcal of carbs, ie people are now eating non-rice carbohydrate. The authors didn't comment on this. I don't suppose anyone who considers saturated fat to be the reason for elevated cholesterol would consider fructose, probably via sucrose, to have any relevance to cholesterol levels.

My guess is that 8 teaspoons a day of sugar is enough to both do some glycation of LDL and to put enough fat in to the liver to raise hepatic insulin resistance. Probably not enough to increase heart attack risk, just enough to raise LDL cholesterol. Not enough to cause hyperglycaemia. Just looking at the numbers needing hypertension meds (see below) I would expect HbA1c to have begun to rise after 1982. Of course sons of Keys would never think to look at HbA1c evels. Too suggestive of Prof Yudkin's ideas!

Is there any other support for the idea of progressively increasing insulin resistance? Back in table 3 we can see that BP is remarkably stable but there is a sudden increase in the percentage of the population needing hypertension medication to achieve this, from 7% in 1989 to 20% in 1999. The roll of elevated insulin in hypertension is not particularly contentious. If you had to say anything about overall health this line tells me that some sort of threshold was crossed in the 1990s. So where are the heart attacks?

Smoking started to fall around 1980, from around 70% of adults (Kitavan levels!) to 45% in 1999. There was zero drop in heart attack rate with this fall. Why not? Perhaps replacing nicotine with fructose is a balanced trade off!

Now, just to finish, TC levels skyrocketed from 152mg/dl in 1958 to 194mg/dl in 1999 and there was no effect on the incidence of coronary heart disease.

How do the jokers running this cohort view their data, which destroy the hypothesis on which their jobs depend?

"In conclusion, large changes in dietary patterns and remarkable changes in serum cholesterol levels among men aged 40-64 years in a Japanese farming area were demonstrated. Fortunately, incidence of coronary heart disease has not increased in our cohort for a couple of decades. The varied composition of the Japanese diet has probably prevented coronary heart disease. However, careful surveillance is needed in the future because of the increasing intake of fat, especially saturated fatty acids, with the potential of a modern epidemic of coronary heart disease in Japan."

The end.

Cholesterol skyrockets, CHD doesn't. A paradox. Unless Keys was wrong and his "offspring" are still wrong.

Oh, or the "varied composition" of the Japanese diet, of which 1000kcal/d is white rice, saves them (giggle, hysterical) from CHD!

10 comments:

Hi Peter - Just a minor correction. Rice is about 72% starch by weight, 28% indigestible fiber. So 593 g/d of rice is 1700 kcal, which would leave 683 kcal from non-rice sources. In the later group you don't give the weight of rice but I'm guessing you may have overestimated rice calories / underestimated sugar calories again. However, there are non-rice sources of starch in Asian diets, also they drink rice drinks (rather like westerners drink soda) which may not have been counted among the rice intake.

The strange calorie/carb difference for the 1958 numbers might be explained thusly:

Rice also contains protein and trace amounts of fat. From some numbers pulled off a nutrition label, in 2668cals of rice there's about 234 cals or so of protein/fat. That should put the numbers a little closer...

Although, when I tried to calculate the calories of 593 grams of rice from this same label, I got 771 calories. Then I realize this is measuring cooked rice. 2126 is the number for uncooked...still 500 calories shy. In that case, there would be 13g protein per cup, and 1g fat as opposed to 4.4 and .4 in cooked rice.

Not going further; my brain short-circuits too easily before noon. I think you got the idea: extra calories are from protein and fat in rice...maybe?

Speaking of cooked versus uncooked rice and calories, etc., I found this to be an interesting "read" and yet another supposition regarding how and why we developed the way we have as humans. Here goes:

I do remember Michael Eades talking about two phases in human brain size increase, first from meat then from cooked meat. So long as no one is suggesting we need porridge for brain power, I'm happy. In fact the further back cooking goes the happier I am with my roast lamb....

I'm about halfway through the Wrangham book on fire & cooking. Interesting book.

Actually, now I remember something about the book I wanted to ask you, Peter. In the book Wrangham mentions studies that show animals become fatter if they eat their food cooked instead of raw food. Do you agree about the weight gain? Pottenger's cat studies come to mind, but I don't recall weight gain being mentioned as an effect of cooked foods.

Anna, it's not something I see. Back in my early days of LC I was trying to work out how much LC tinned cat food would be the equivalent of the calorie count of Cr@pinabag slimming diets to get weight loss on my obese feline patients. The can of Arthurs (Nestle, Peter vomits in the corner) I checked gave no calorie content and just said feed ad lib and your cat will select its food intake for normal weight. Works fine as far as I can see. There might be other issues with AGEs and cats but I don't see weight gain as one of them. Back when I did routine medicine few clients would do rawfeeding but most would feed ordinary canned LC food. Not as good for overall health but pretty effective for weight loss (I found only rawfeeding really worked for hypertensive cats, tinned food didn't do as well, but my number of cases was small).

Of course it depends what you are cooking and what you are feeding raw. Raw, uncooked, unground, whole wheat kernels would be great for weight loss in cats. Just poop scoop them out of the litter tray and plant them in a field for next years premier weight loss cat food!

I do think physical labor is a huge factor in why people are hyperinsulinemic and fat today.

In my experience anyway, even relatively small differences in activity make a huge difference in metabolism. Lowering glucose (even causing hypoglycemia, non reactive type) and allowing me to tolerate more carbs and such. Not become of some dumb "cal in cal out" idea but because of how it is verified that physical activity makes big differences in insulin levels during the day.

Re: fat kitties. My little kitty gets rapidly fat when I feed him food that contains more than 10% carb. He is a thin cat and tends toward poor appetite (unless I feed him canned 90% meat fancy feast or something else that probably has some kind of appetite stimulant in it)... but when I give him the canned varieties with a higher percentage of carb, or god forbid dry food, he starts becoming torporous and lays on a nice pad of fat under his skin. To tell you the truth I like him chubbier, but the lethargy is unfortunate.

For my cat anyway, even relatively low carb cat foods affect his weight and energy, he has the most energy (and is the thinnest and eats less) when he has the lowest carb varieties.

To counteract the effect of excessive skinniness, roaming too much and being a loud ass annoying cat, I give him fancy feast ocean whitefish as he eats this a lot even though it is really low in carb... which helps keep his weight up and it keeps him more mellow, but it doesn't cause that unhealthy "100% fat" type weight that goes along with sedation that the dry food gives him.

I also got some vitamins for cats and that made a big deal in his appearance and coat.

You put forth the notion that insulin resistance is caused by fructose. I wonder what your take is on this study, in which subjects significant lowered their fasting insulin following a "paleo" diet containing massive amounts of fructose:

About Me

I am Petro Dobromylskyj, always known as Peter. I'm a vet, trained at the RVC, London University. I was fortunate enough to intercalate a BSc degree in physiology in to my veterinary degree. I was even more fortunate to study under Patrick Wall at UCH, who set me on course to become a veterinary anaesthetist, mostly working on acute pain control. That led to the Certificate then Diploma in Veterinary Anaesthesia and enough publications to allow me to enter the European College of Veterinary Anaesthesia and Analgesia as a de facto founding member. Anaesthesia teaches you a lot. Basic science is combined with the occasional need to act rapidly. Wrong decisions can reward you with catastrophe in seconds. Thinking is mandatory.
I stumbled on to nutrition completely by accident. Once you have been taught to think, it's hard to stop. I think about lots of things. These are some of them.

Organisation (or lack of it)!

The "labels" function on this blog has been used to function as an index and I've tended to group similar subjects together by using labels starting with identical text. If they're numbered within a similar label, start with (1). The archive is predominantly to show the posts I've put up in the last month, if people want to keep track of recent goings on. I might change it to the previous week if I ever get to time to put up enough posts in a week to justify it. That seems to be the best I can do within the limits of this blogging software!